Approximately 50% of infants born with congenital heart disease have or will develop significant cyanosis requiring therapeutic intervention. The neurologic effects of prolonged cyanosis produced by congenital heart of chronic cyanosis on cerebral metabolism in the neonatal lamb. Two groups of animals (n=15 each) have been studied. Initial P-31 NMR spectra were measured at the age of 10 days. Following creation of a miocardial right-to-left shunt (experimental group) or sham thoracotomy (control group) at the age of two weeks, serial brain NMR spectra were obtained at monthly intervals. Despite signifiant differences in arterial blood oxygenation in two groups (cyanotic vs, control), no differences were found in high energy phosphates (ATP, phosphocreatine and inorganic phosphate), their ratios (PCr/ATP, PCr/Pi, and PCr/PME) and brain tissue pH. The data from this study shows no changes in intracerebral phosphate metabolism and pH in response to chronic hypoxia in an in-vivo model of cyanosis, and thus does not provides guidance to tha answer of the important question of when to intervene in patients with correctable cyanotic heart disease via surgery.